PPARfJ involved in endothelial cell injury induced by high glucose via nitrative stress
- Author:
Chuang YANG
1
;
Bao-Ping XIONG
1
;
Yun-Dan ZHENG
1
;
Si-Man LI
1
;
Shang-Jun ZHOU
1
;
Qing-Song JIANG
1
Author Information
- Publication Type:Journal Article
- Keywords: 3-nitrotyrosine; endothelial cells; high glucose; injury; nitrative stress; PPARβ
- From: Chinese Pharmacological Bulletin 2022;38(6):848-853
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the role of PPARβ and nitrative stress in human umbilical vein endothelial cells(HUVECs)injury induced by high glucose.Methods The cell viability was detected by CCK-8.The cell proliferation was detected by EdU proliferation detection kit.The protein expression level of PPARβ,eNOS,iNOS,and 3-nitrotyrosine was detected by Western blot.The content of peroxynitrite and nitric oxide(NO)was determined by peroxynitrite kit and Griess Reagent,respectively.Results Glucose(30,40,50 mmol·L-1)significantly reduced the cell viability of HUVECs in a dose-dependent manner.Glucose at 30 mmol·L-1(high glucose,HG)significantly reduced the proliferation of HUVECs,down-regulated the expression of PPARβ,eNOS at protein level and NO content,and increased iNOS,3-nitrotyrosine protein expression and peroxynitrite level.The above effects of HG were reversed by PPARβ agonist GW0742(1 μmol·L-1).Both PPARβ antagonist GSK0660(1 μmol·L-1)and NOS inhibitor L-NAME(10 μmol·L-1)blocked the protective effects of GW0742.Conclusion The down-regulation of PPARβ is involved in the injury of HUVECs induced by high glucose,which may be mediated,at least partly,by the stimulation of nitrative stress.
